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营养不良小鼠肌肉抽搐减缓部分是由于活动模式改变。

Slowing of twitch of dystrophic mouse muscle in partially due to altered activity pattern.

作者信息

Parry D J, Desypris G

出版信息

Muscle Nerve. 1983 Jul-Aug;6(6):397-407. doi: 10.1002/mus.880060602.

Abstract

Fast-twitch muscles of the hindlimb of dystrophic (dy2J) mice show a prolongation of both the contraction and relaxation phases of the isometric twitch. Comparable muscles of the forelimb of these mice exhibit relatively little increase in time to peak tension but time to half-relaxation is as severely affected as in the hindlimb. When examined with an immunohistochemical technique to demonstrate the presence of "slow" myosin it was apparent that there were no fibers containing the "slow" isoenzyme in either hindlimb or forelimb muscles of 6-month control mice. In dy2J mice hindlimb muscles contained many fibers with "slow" myosin whereas forelimb muscles did not. It is suggested that the spontaneous twitching activity produced in the hindlimbs, as a result of amyelination of the spinal roots, induces synthesis of "slow" myosin, which in turn leads to prolongation of time to peak twitch tension.

摘要

营养不良(dy2J)小鼠后肢的快肌在等长收缩时,收缩期和舒张期均延长。这些小鼠前肢的相应肌肉在达到峰值张力的时间上增加相对较少,但半舒张时间与后肢一样受到严重影响。当用免疫组织化学技术检测以证明“慢”肌球蛋白的存在时,很明显6个月大的对照小鼠的后肢和前肢肌肉中都没有含有“慢”同工酶的纤维。在dy2J小鼠中,后肢肌肉含有许多具有“慢”肌球蛋白的纤维,而前肢肌肉则没有。有人认为,由于脊髓神经根脱髓鞘,后肢产生的自发抽搐活动会诱导“慢”肌球蛋白的合成,进而导致达到抽搐峰值张力的时间延长。

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